Upper GI Disorders - Oesophagus, Stomach, Pancreas Flashcards
(20 cards)
Anatomy of the oesophagus and gastro-oesohageal junction
Upper third → striated muscle, vagal motor innervation
Lower two thirds → smooth muscle, continuous with stomach. Vagal parasympathetic innervation
Oesophageal motility
Upper oesophageal sphincter relaxation → brief as bolus passes through
Relaxation of the oesophageal body and LOS → nitric oxide, VIP. LOS relaxes to intragastric pressure
Coordinated contraction of smooth muscle of the oesophagus → acetylcholine
Risk factors for gastro-oesophageal reflux
- Age
- Obesity
- Hiatus hernia
- Pregnancy
- Specific conditions → scleroderma, asthma
- Smoking, alcohol
H. pylori protective
Complication of reflux disease
Ulceration/bleeding
Stricture/Schatzki ring
Barrett’s oesophagus
Adenocarcinoma of oesophagus
Extra-intestinal manifestations - pharyngeal reflux
Epidemiology of reflux disease, symptoms, and symptoms of complications
- Common - 40% ever
- West>East, developed > developing
- Symptoms not a predictor of oesophagitis - severity of heartburn similar in patients with different grades of oesophagitis
Symptoms
Heartburn, regurgitation
Nonspecific → nausea, epigastric pain, respiratory (cough, worsening asthma), ENT, dental, chest pain, sleep disturbance
Symptoms of complications
Dysphagia - oesophagitis, stricturing, malignancy
Haemetemesis
Weight loss
Diagnosis of GORD
Clinical diagnosis
Endoscopy only if atypical symptoms, poor response to treatment, red flags → 50% endoscopy negative
PH/impedence studies
Endoscopy
Severity of oesophagitis - Los Angeles A→ D
Presence of hiatus hernia
Presence of Barrett’s
Presence of other conditions that may mimic or exacerbate reflux symptoms
Management of GORD
- Lifestyle → lose weight, avoid fatty/spicy food, avoid late meals, elevate head of bed, antacids, avoid alcohol, citrus fruits may also aggravate
- PPIs - start high dose then titrate down
- H2 receptor antagonists (PPIs more effective in terms of healed eosophagitis)
- Prokinetics
- ?Trial of TCA
Medications that may aggravate GORD
Impaired LES function → beta agonists, theophylline, anticholinergics, TCAs, calcium channel blockers, progesterone, alpha adrenergic antagonists, diazepam
Damage to oesophageal mucosa → aspirin, NSAIDs, doxycycline, quinidine, bisphosphonates
Inidications for surgery and options in GORD
- Failed medical management
- Medication non-compliance
Fundoplication - laparoscopic or open
- Side effects → ++flatus, limited period of dysphagia
- Occasional → severe dysphagia, gas bloat, inability to belch, vomit. Paraoesophageal hernia
- Failure with time
Notes on Barrett’s oesophagus - definition, epidemiology
- Metaplasia of variable distance of lower oesophagus to mucosa of cardia, gastric or intestinal type
- Increases with age - 1-2% population, 10% reflux patients
- Risks:
- Male
- Caucasian
- Severe reflux symptoms → prevalence increases with duration of reflux symptoms
- Increased incidence of oesophageal adenocarcinoma → lesions >3cm associated with higher risk
Screening and management of Barrett’s oesophagus
Screening
- No proven benefit but if found needs biopsy confirmation → best taken after healing (inflammatory changes interfere with assessment of dysplasia)
Management
- Management of oesophagitis and symptoms
- Manage risk of malignancy → surveillance programme
- No dysplasia → 3-5 years
- Low grade → 6 month
- High grade → see below
High grade dysplasia
- Mucosal ablation combined with PPI can elimate macroscopic Barrett’s (submucosal islands may persist)
- Reduced incidence of oesophageal adenocarcinoma (in high grade group only)
- If young and multifocal disease may need to consider oesophagectomy (1-20% mortality however, risk and benefit needs to be balanced)
Manifestations of coeliac disease
Iron deficiency
Osteoporosis
Hypocalcaemia
Late menarche, early menopause, miscarriages, secondary amenorrhoea, infertilty, preterm delivery and low birth weight
Notes on primary biliary cirrhosis
- Most common presenting symptom fatigue and pruritus
- Presence of symptoms worsens prognosis - 50% asymptomatic
- Positive antimitochondrial antibody
- No role for treatment if normal LFTs
- Ursodeoxycholic acid used in treatment
Mechanism of aspirin/NSAID induced peptic ulcer disease
- COX 2 inhibition → decreased prostaglandins
Notes on gastrinomas/Zollinger-Ellison syndrome
- Diagnosed with secretin stimulation test → differentiate patients with gastrinomas from other causes of hypergastrinaemia (e.g. in the setting of gastrin < 10 times ULN, and gastric pH ≤2
- Secretin stimulates release of gastrin by gastrinoma cells, patients with ZES tumours → dramatic rise in serum gastrin. Normal gastric G cells inhibited by secretin
- Should not be performed on patients on PPI therapy → false negative up to 20%, false positive up to 40%
Notes on achalasia - symptoms and investigations
- Incomplete LOS relaxation → Oesophageal aperistalsis → replaced by undulating “common cavity” pressure waves due to ineffective contractions
- Loss of inhibitory neurotransmission → ?autoimmune precipitated by viral infection
- Heterogeneous condition
- Symptoms → dysphagia (solids & liquids, progressive +/- weight loss), regurgitation (postural → night), chest discomfort/pain (may simulate heartburn)
- Endoscopy → food in oesophagus, tight LOS, dilated oesophagus, done to exclude stricturing lesions
- CXR → Lack of gastric air bubble, retrocardiac fluid level
- Barium swallow → birds beak, holdup in dilated oesophagus, aperistalsis
- Manometry → most sensitive, imcomplete LOS relaxation
Management of achalasia
- Medications → GTN, calcium channel antagonists (generally not effective)
- Balloon dilation → controlled rupture of LOS, 3-5% perforation rate, variable success rate
- Botox → injected into LOS, 70% success, needs repeating after 3-6 months
- Myotomy → surgical division of LOS, laparoscopic. Highly effective, low morbidity.
- POEM (per oral endoscopic myotomy), PEG, oesophagectomy other options
Notes on acute pnacreatitis
Amylase
- Half life 10 hours
- >3x ULN sensitivity of 67-83%, specificity 85-98%
- Low in: alcoholics, hypertriglyceridaemia
- High in: DKA, ARF, parotid disease, malignancy, other
Lipase
- Peaks at 24 hours, returns to normal in 8-14 days
- High inL renal failure, DU, DKA, HIV, coeliac disease, other
- Mild = no organ failure
- Moderately severe = > 48 hours organ failure or local/systemic complications
- Severe = persistent organ failure
Complications of acute pancreatitis
Acute peripancreatic fluid collection
- Extra-pancreatic, no wall
- No necrosis or solid material
Psuedocysts
- Mature fluid collections outside the pancreas at least four weeks out
- Well defined wall
- No necrosis or solid material
Acute necrotic collection
- Adjacent to or involving the pancreas
- No wall
- Liquid and solid material
Walled off pancreatic necrosis
- Mature encapsulated necrosis with solid and liquid elements
- Intra- or intrapancreatic
Notes on chronic pancreatitis
- Progressive fibroinflammatory process → permanent structural damage and impairment of exocrine or endocrine function
- Complications → psuedocyts (10%), bile duct or duodenial obstruction (5-10%), pancreatic ascites, splenic vein thrombosis and psuedoaneursyms
- Differs from acute pancreatitis:
- May be asymptomatic over long periods
- Enzymes tend to be normal
- Patchy focal disease with fibrosis
Causes
- Alcohol
- Genetic - CFTR, SPINK1
- Ductal obstruction (stone, trauma, psuedocyst)
- Tropical pancreatitis
- Autoimmune pancreatitis
- Systemic diseases → SLE, hyperparathyroidism
- Idiopathic
Features of chronic pancreatitis and treatment
Features
- Abdominal pain
- Pancreatic insufficiency
- Exocrine (>90% pancreas lost)
- Endocrine (increased risk of hypoglycaemia due to loss of alpha cells)
Diagnosis difficult - lab tests and imaging can be normal
MRI best imaging modality
Dx strongly suggested by pancreatic calcification, steatorrhoea, and DM
Faecal elastase most sensitive and specific lab test
Selective genetic testing - CFTR, SPINK1, PRSS 1
Treatment
- Pain management
- Stop alcohol, smoking
- Hydration, small meals
- Analgesia - opiates, NSAIDs, pregabalin, endoscopic therapy, coeliac plexus block, surgery
- Correction of pancreatic insufficiency
- Lw fat diet
- Enzyme supplementation
- Medium chain triglycerides
Notes on autoimmune pancreatitis
- Rare
- Painless jaundice
- Clinically and radiologically difficult to distinguish from pancreatic cancer
- Dramatic response to glucocorticoids
- Untreated can → pancreatic failure
